Babesia: The malaria-like disease in your yard, part 1

It was sometime after the New Year when, feeling better but hardly well after initial treatment for Lyme disease, that I drove a mile down my hill for a latte at Starbucks and my appointment with my Lyme practitioner. She greeted me with a smile, waving a paper in my face. She seemed so pleased she was literally aglow.

A few weeks before, dissatisfied with a plateau in my treatment response, my returning migraines and fatigue, she'd drawn blood and sent it to Quest Lab for a babesia test. "When Lyme disease patients don't get well," she told me, "coinfection with babesiosis is often the cause." Now the results had come back, and as with my Lyme ELISA, antibodies werefour times the cutoff for positive-sky-high.

The pieces were falling into place. With my spiking headache and continued exhaustion, babesiosis certainly made sense for me. A decade earlier, in 1990, I'd spent a couple of weeks as a science-writing fellow at the Marine Biological Laboratory at Woods Hole, Massachusetts, right across the water from Nantucket lsland, where human babesiosishad been studied more than fifteen years before.

It was during the early seventies, before Lyme was even recognized, that Andrew Spielman, a tropical medicine expert at the Harvard School of Public Health, was asked to investigate what locals called Nantucket fever. At the time, only two patients were known. The first was a wealthy Nantucket woman who came down with a disabling mystery illness marked by extreme anemia, fatigue, and fever that local doctors could not explain. So she chartered a plane to Rutgers, New Jersey.

Rutgers doctors examined her blood under a microscope, diagnosed her with malaria, and placed her on the standard treatment, chloroquine. When the treatment didn't work, they grew alarmed because drugresistant malaria is, after all, a threat to public health. A slide of blood was shipped off to the CDC, where experts identified not malaria but another similar agent that also inhabits red blood cells-Babesia microti, known to cause cattle epidemics that wiped out entire herds. With the identification of her infection, the woman was finally treated correctly and got well.

When a second case of babesiosis appeared on Nantucket Island a few years later, physicians again were stymied. But the second patient happened to be friends with the first, and finally, with doctors throwing up their hands, it fell to the first patient to diagnose the disease in the second. Her lay diagnosis was correct, and the second patient wastreated and recovered as well.

That's when Spielman entered the fray. Would he care to find the cause of these cases in the environment? Observing the cycles of infection year after year, he finally tracked babesia through the ecosystem, discovering that it lived in the blood of mice and spread from one mammal to the next through the bite of an Ixodes tick. Larva and nymphal (baby and adolescent) ticks ate by sucking the blood of mice and other small mammals like shrews and chipmunks. But adult ticks, far bigger in size, generally required larger mammals like deer for a blood meal. It was only in geographic areas with an abundance of large mammals that Ixodes ticks could mature to adulthood and reproduce substantiallyenough for the disease to spread.

When the spirochete Borrelia burgdorferi was identified by Willy Burgdorfer as the cause of Lyme disease in 1981, Spielman realized that the newly discovered illness involved the same tick and same natural cycle he'd already charted for human babesiosis on Nantucket Island and beyond. For Spielman, the connection between the two infections-Lyme and babesiosis-was immediately clear. Every year since his first discoveries on Nantucket, after all, new babesia patients had been diagnosed.

And some of them had exhibited not just the malarialike headache and fever spikes typical of babesia, but also a confounding circular red rash and strange pains that migrated from joint to joint-symptoms classically associated not with babesiosis, but rather Lyme disease. "There was a woman who lived opposite our field station who had migratory arthritis and the expanding rash and-babesiosis. She obviously had Lyme as well, but no one had the organism, and restrictive case definitions came into play," Spielman recalled, "because in the beginning, the differential diagnosis for Lyme disease included a travel history to Lyme, Connecticut!"

Eventually the boundaries for both infections expanded at different but proportional rates, and with each infection requiring a treatment ineffective for the other, the coinfected patients of Nantucket Island provided important clues to the spectrum of disease. Sometimes physicians just needed to treat babesiosis for an intractably sick "Lyme" patient to get well. Even as babesiosis extended its range and came to rival Lyme disease as a cause of illness, the lessons of Nantucket's coinfected patients would fall on deaf ears.

Indeed, few Lyme disease patients were ever tested for, or had even heard of, babesiosis; and though the two epidemics had been spawned in tandem from the start and could be equally debilitating, few primary care doctors in endemic areas ran the babesiosis test. "We don't test for that," our Westchester county pediatrician explained at the time.The internist who tried to treat my headaches-classic for babesiosis- never mentioned the possibility that infection, either Lyme or babesiosis, might be a cause.

Yet in retrospect I believe the Babesia diagnosis was my missing link. Most science-writing fellows at Woods Hole had stayed in residence halls near the lab, but with a family in tow I was given a gorgeous rustic cabin in the woods. Way before my arrival, Babesia microti had begun its migration west and south, first over Cape Cod and then down the Long Island Sound, fast on the heels of Lyme disease toward Connecticut, Westchester, and the points beyond. In 1990, still traveling incognito toward New York State, Babesia microti was already rife in the forested enclaves of Woods Hole.

It wasn't just my exposure that fit with the Quest results, but the mystery illness I'd suffered after returning from Cape Cod. Doctors could never explain the strange spikes of fever to 105 degrees Fahrenheit that hit me in hallucinogenic waves for more than a week that summer, or the gullies of sleep so black that, except for the nightmares, I thought I might be dead. When the fever broke and I noticed the sweating, it seemed just a consequence of summer. It was after the sweat leveled off that the headache-without-end licked its first noxious path through my brain.

This was classic acute babesiosis. Without treatment the acute infection had flared and apparently smoldered, my Lyme practitioner theoriezed. Then it had synergized in concert with the Lyme.

She had a treatment to push the babesia back: I now added Mepron to my arsenal of antibiotics. The thick gold sludge, known for treating malaria, made me retch and want to vomit. But I held it down. Some six weeks later, the drill in my head stopped whirring and the nausea and dizziness I'd lived with for years receded like a tide pulled back to sea. I still wasn't better, not entirely, but we had peeled another layer off the onion and extinguished another set of symptoms from my disease.

Pamela Weintraub is a Senior Editor at Discover Magazine. The post above is adapted from her book on Lyme disease and its coinfections, entitled Cure Unknown: Inside the Lyme Epidemic, published in 2008 by St. Martin's press.

breaking this up for all of us neuro lyme/co-infection patients who can not read or comprehend long solid text paragraphs.

when you reply, we sure would appreciate short sentences so we can follow the ENTIRE feedback of all repliers. god bless you all for helping us neuro folks who are challenged enough daily! :) xox

Babesia: The malaria-like disease in your yard, part 1
By Pamela Weintraub
on April 4, 2009 - 5:09pm in Emerging Diseases

It was sometime after the New Year when, feeling better but hardly well after initial treatment for Lyme disease, that I drove a mile down my hill for a latte at Starbucks and my appointment with my Lyme practitioner. She greeted me with a smile, waving a paper in my face. She seemed so pleased she was literally aglow.

A few weeks before, dissatisfied with a plateau in my treatment response, my returning migraines and fatigue, she'd drawn blood and sent it to Quest Lab for a babesia test.

"When Lyme disease patients don't get well," she told me, "coinfection with babesiosis is often the cause." Now the results had come back, and as with my Lyme ELISA, antibodies were four times the cutoff for positive-sky-high.

The pieces were falling into place. With my spiking headache and continued exhaustion, babesiosis certainly made sense for me.

A decade earlier, in 1990, I'd spent a couple of weeks as a science-writing fellow at the Marine Biological Laboratory at Woods Hole, Massachusetts, right across the water from Nantucket lsland, where human babesiosis had been studied more than fifteen years before.

It was during the early seventies, before Lyme was even recognized, that Andrew Spielman, a tropical medicine expert at the Harvard School of Public Health, was asked to investigate what locals called Nantucket fever.

At the time, only two patients were known. The first was a wealthy Nantucket woman who came down with a disabling mystery illness marked by extreme anemia, fatigue, and fever that local doctors could not explain.

So she chartered a plane to Rutgers, New Jersey.

Rutgers doctors examined her blood under a microscope, diagnosed her with malaria, and placed her on the standard treatment, chloroquine.

When the treatment didn't work, they grew alarmed because drugresistant malaria is, after all, a threat to public health.

A slide of blood was shipped off to the CDC, where experts identified not malaria but another similar agent that also inhabits red blood cells-Babesia microti, known to cause cattle epidemics that wiped out entire herds. With the identification of her infection, the woman was finally treated correctly and got well.

When a second case of babesiosis appeared on Nantucket Island a few years later, physicians again were stymied.

But the second patient happened to be friends with the first, and finally, with doctors throwing up their hands, it fell to the first patient to diagnose the disease in the second.

Her lay diagnosis was correct, and the second patient was treated and recovered as well.

That's when Spielman entered the fray. Would he care to find the cause of these cases in the environment?

Observing the cycles of infection year after year, he finally tracked babesia through the ecosystem, discovering that it lived in the blood of mice and spread from one mammal to the next through the bite of an Ixodes tick.

Larva and nymphal (baby and adolescent) ticks ate by sucking the blood of mice and other small mammals like shrews and chipmunks.

It was only in geographic areas with an abundance of large mammals that Ixodes ticks could mature to adulthood and reproduce substantially enough for the disease to spread.

When the spirochete Borrelia burgdorferi was identified by Willy Burgdorfer as the cause of Lyme disease in 1981, Spielman realized that the newly discovered illness involved the same tick and same natural cycle he'd already charted for human babesiosis on Nantucket Island and beyond.

For Spielman, the connection between the two infections-Lyme and babesiosis-was immediately clear. Every year since his first discoveries on Nantucket, after all, new babesia patients had been diagnosed.

And some of them had exhibited not just the malarialike headache and fever spikes typical of babesia, but also a confounding circular red rash and strange pains that migrated from joint to joint-symptoms classically associated not with babesiosis, but rather Lyme disease.

"There was a woman who lived opposite our field station who had migratory arthritis and the expanding rash and-babesiosis.

She obviously had Lyme as well, but no one had the organism, and restrictive case definitions came into play," Spielman recalled, "because in the beginning, the differential diagnosis for Lyme disease included a travel history to Lyme, Connecticut!"

Eventually the boundaries for both infections expanded at different but proportional rates, and with each infection requiring a treatment ineffective for the other, the coinfected patients of Nantucket Island provided important clues to the spectrum of disease.

Sometimes physicians just needed to treat babesiosis for an intractably sick "Lyme" patient to get well.

Even as babesiosis extended its range and came to rival Lyme disease as a cause of illness, the lessons of Nantucket's coinfected patients would fall on deaf ears.

Indeed, few Lyme disease patients were ever tested for, or had even heard of, babesiosis; and though the two epidemics had been spawned in tandem from the start and could be equally debilitating, few primary care doctors in endemic areas like Chappaqua ran the babesiosis test.

The internist who tried to treat my headaches-classic for babesiosis- never mentioned the possibility that infection, either Lyme or babesiosis, might be a cause.

Yet in retrospect I believe the Babesia diagnosis was my missing link. Most science-writing fellows at Woods Hole had stayed in residence halls near the lab, but with a family in tow I was given a gorgeous rustic cabin in the woods.

Way before my arrival, Babesia microti had begun its migration west and south, first over Cape Cod and then down the Long Island Sound, fast on the heels of Lyme disease toward Connecticut, Westchester, and the points beyond.

In 1990, still traveling incognito toward New York State, Babesia microti was already rife in the forested enclaves of Woods Hole.

It wasn't just my exposure that fit with the Quest results, but the mystery illness I'd suffered after returning from Cape Cod.

Doctors could never explain the strange spikes of fever to 105 degrees Fahrenheit that hit me in hallucinogenic waves for more than a week that summer, or the gullies of sleep so black that, except for the nightmares, I thought I might be dead.

When the fever broke and I noticed the sweating, it seemed just a consequence of summer. It was after the sweat leveled off that the headache-without-end licked its first noxious path through my brain.

This was classic acute babesiosis. Without treatment the acute infection had flared and apparently smoldered, my Lyme practitioner theoriezed. Then it had synergized in concert with the Lyme.

She had a treatment to push the babesia back: I now added Mepron to my arsenal of antibiotics. The thick gold sludge, known for treating malaria, made me retch and want to vomit. But I held it down.

Some six weeks later, the drill in my head stopped whirring and the nausea and dizziness I'd lived with for years receded like a tide pulled back to sea.

I still wasn't better, not entirely, but we had peeled another layer off the onion and extinguished another set of symptoms from my disease.

Pamela Weintraub is a Senior Editor at Discover Magazine.

The post above is adapted from her book on Lyme disease and its coinfections,
entitled Cure Unknown: Inside the Lyme Epidemic, published in 2008 by St. Martin's press.

Pam, another outstanding article educating all of us about the CO-INFECTIONS that you get also from ticks, etc.

I learned a lot from your above post as I don't have bart or babs as co-infections.....lucky me!

I broke it up above but I need to enlarge the font to largest size for my LOW vision, so could not reply without having a post where I can read the entire line vs. 50-60% of it only.

I've had chronic lyme for 39 years; 34.5 years misdiagnosed by 40-50 drs. In the last almost 5 years I have educated myself galore about lyme and the "normal" coinfections that you can get: babsesiosa, bartonella, ehrlichia, rocky mountain spotted fever, and the list goes on and ON!

Since then, I learned my late Dad had UNDIAGNOSED lyme and co-infections for 80 years of his life of 86 years! I witnessed the symptoms and diseases that mimick lyme/co-infections; oh brother, over 300 of them overlap!!

He was bitten by a tick then at age 6; his Mom drove him to Mud Springs, Minn. where he spent 1 month there in their hot mineral waters helping the severe arthritis he had gotten.

Twice in his life, he was paralzed from the neck down! Twice he came OUT OF IT being able to use his body fully.

Once was another co-infection, BLASTOMYCOSIS, that paralyzed him, and he was in the hospital for 1 month. I remember Mom sneaking us in the back door of hospital so we 3 kids then could visit a little with him.

When he came home, he had to drink pure iodine several times a day for an unknown length of time since I was only 6-8 years old then.

He couldn't reach across the table to even get a raw cut up carrot to eat.

Over the years, more advanced lyme/co-infections hit him and not ONCE in his 80 years of being a chronic lyme/co-infection patient, NO DR. MENTIONED BEING BITTEN BY A TICK and possible lyme/co-infections! He'd seen over 100 - 150 drs. during his lifetime.

I'm sorry, Pam's writing above brought back memories to me now, so I decided to share them with you all as well.

Pam, please keep educating US ALL; those of us who have these diseases, and the large medical profession.

We affected patients need to be taken serious and not chided and told, "it's all in your head"! It's not ...the spirochetes have invaded our entire body!!

Pam, thank you for your well-written words and thought-provoking observsations !~! We are truly blessed to have you as a lyme/co-infection spokeswoman :) xox

I would say that it did work because he lived to be very old. I have no idea how much he took, if he took enough to discourage the buggers. I found Lugol's to be very effective. My view is that people get lyme because they are deficient in iodine but I have no proof for that view and no one is talking about it.

Your article has brought such light to my disease and struggles over the last 30 yrs. I too contracted lyme disease while vacationing on Nantucket Island during the late 1970's.

I came home from vacation and had the typical bullseye rash and all of the text book symptoms to follow. My pediatrician worked hard on trying to figure out what I had but came to the conclusion that I possible had JRA.

Fast forward 29 yrs later, finally I was diagnosed and I am now being treated.

After reading this article I only wished we knew about Rutgers Dr's considering I am just 20 minutes away from them. My life could have turned out so differently.

I was diagnosed at 22 with lyme and was sent to Dr Sigal at the Robert Wood Johnson Medical Department. But, I do not consider this any kind of treatment due to how he handled me.

He put me on a months worth of abx's and after the month was up I told him that the symptoms were coming back and cut me off and told me I was cured and I now have fibromyalgia. Here take these pills at bed and you will be better.

I threw that prescription away due to not liking or trusting him at all. He never even explained to me what fibro was. He just rushed me out of his office. I have now come to find out just how intertwined he is with the drug companies. Also that he didn't consider himself an authority on infectious diseases. Funny, since that is why I was sent to him.

I will be taking this article to my llmd and show him it because I have tested negative for co infections. Headaches have been one of my biggest problems.

Thank you so much again for helping us with your insight and research that you do that allows us to educate ourselves more on our disease.

I live in California. I was hospitalized for 5 days with exteme high fever, sweats and a horrible headache. They never did figure out what was wrong, except for a nurse who told me, "if I didn't know any better, I'd say you had malaria". The hospital never tested me for any tick infection, despite the fact that ticks in the area carry these diseases. Unfortunately, the hospital, the only one in the county, has as its president an Infecticious Disease MD, who had infamously said several years earlier, "There is no such thing as lyme in California."

Two years later, a doctor finally diagnosed me with both lyme and babesea. When I told my other doctors, they said, "that's impossible, babesea is very rare, and only occurs in certain small areas of the northeast. And we don't have lyme here either."

Pam,
thank you for sharing your story. So many people still sick with lyme and don't know why. The co-infections- which do NOT normally show up on Quest or even "good" highly specific labs (I personally was NEGATIVE 5x using the most sensitive test available), but the symptoms are So abundantly clear. The sweats, headaches, fatigue, etc. Worst of all, so few get tested for Babesia DUNCANI, which even kills rats! There is only one author who has published anything on this topic - and his current 3 books are what helped me find treatment that works - can be seen at www.personalconsult.com. Most LLMD's know nothing about the co-infections. A real shame as people just stay sick, lose marriages, jobs, etc. when they could be getting better!
Your courage in pursuing this topic is much appreciated.

We live in Missouri. We believe that my husband has Lyme Disease. He was bitten about a year ago, all the classic systoms, bulle eye rash, fever, extreme fatigue, headaches and joint pain,ankles. After months of reading, we now understand WHY the doctors are afraid to say that yes, it is Lyme . We had no idea why the doctors refuse to even believe that Lyme is a possiblablity. It is more clear now after all the articles that we have come across. It is unbelievable how long some people have suffered. We pray that help is on the way. Thank-you for some much valuable infomation. May God bless you.

Just surfing the net. Saw a post in psychologytoday where a woman who couldnt get help in missouri for lyme. you asked her to contact you that there was something that she could do to help others, I assume since she could not get help either. I was curious if there is a way to help others. My story is an absolute nightmare, and getting help was a long drawn out process. Im in treatment now, for about 5 months. I was told that labs made a mistake, even though I was CDC positive, and very very ill.

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Robert asked me to publicize his case, to help others suffering similar symptoms, especially chronic pain, chronic fatigue and fibromyalgia patients still being told, “it is all in your head.”

Robert is Currently Disabled by Babesiosis, Phlebitis and possibly Lymes disease, but is experiencing dramatic decreases in joint and phlebitis pain.

Robert is suffering from Babesiosis and possibly Lymes disease, in addition to a severe Immunoglobin M deficiency, complement dysfunction, phlebitis, hypertension and dyspituitarism. He has also been exposed to the Epstein Barr and Human Herpes 6 viruses, which may also be contributing to his symptoms.

Babesiosis has produced mortality rates as high as 10 percent, in the United States, and 50 percent, in Europe. Although treatment has improved some of his symptoms and he can hopefully expect continued decrease of abnormal sweating, fatigue, memory impairment and joint pain, Robert’s treatment will cause temporary worsening of his symptoms, when antimicrobial medications and herbals are pulsed and cycled to kill microbial pathogens. When treatment kills protozoal and bacterial pathogens their cell membrane ruptures, allowing release of additional toxins which aggravate symptoms to a disabling level, during microbial die-off.

During a microbial die-off, Robert may need to almost totally avoid standing or walking, due to extreme hypersensitivity of his feet to pressure. He will also likely benefit from keeping his feet elevated. Robert also may require three days to recover from even minimal physical exertion, due to deficient Vasoactive Endothelial Growth Factor, VEGF.

During the off cycle of antimicrobial treatment, a prescription medication, Cholestyramine, is used to bind fat soluble toxins. During these periods, Robert can be expected to experience decreased joint pain, swelling, skin sensitivity, and shortness of breath.

He complained of allodynia, especially in hands and feet, arthritis and unusual chills and excessive sweating, alternating between upper and lower body, in addition to muscle pain, fatigue and memory impairments. He reports some of these problems began about 8 years ago after a tick bite and hospitalizations for surgeries. For months, after the tick bite, Robert experienced extreme pain when his hand was touched and had to avoid handshakes. Patient has been on 2 hypertension medications and is currently taking Atacand. Robert voluntarily underwent detoxification for Actiq (Fentanyl) and requested help with hyperhidrosis(excessive sweating) and pain.

Robert reported many frustrating prior experiences with over 50 medical providers who did not find any unusual test results and many who apparently did not believe some of the symptoms he reported. Patient failed Visual Contrast Sensitivity Test (FACT) prior to serum testing. Labcorp testing revealed a highly elevated MMP9 of 1128(should be less than 300). Robert began Cholestyramine and observed decreased pain in his hands.

On 5/29/08 a serum sample submitted to Quest Diagnostics revealed a D-Dimer of 0.54 mcg/ml, considered high, with a normal reference range of 1.0); Serum Immunoglobin M 17(40-230)mg/dl (Hypogammaglobulinemia occurred in approximately 0.5 % of over 13,000 patients, in a published study) ; EBV Early Antigen, Ig G, 106 AU/ml(100-120 equivocal); EBV Early VCA, IgG 1,427 AU/ml (positive > 120); EBV nuclear antigen 1,173 AU/ml (positive >120); The elevated creatine kinase can explain some of the muscle pain Robert suffers.

Robert was instructed to begin New Life Colostrum, to increase immunoglobins and Enzymatic Therapy Cell Forte to increase Natural Killer Cell count and instructed to consult an infectious disease or immunology specialist. He was informed that he might need gamma globulin injections and would need to see a specialist for them. It was also explained that his prior testing for Lymes and Babesia might have given false negatives, since he was very immune suppressed. ACA Ig A,G,M; RPR; CMV IgG; and HSV II were wnl. CD4:CD8 was 2.96; CD4 lymph percentage was 55.4; CD8 lymph percentage was18.7; WBC 6400, neutrophils, 63 %; lymphocytes, 26 %; monocytes were 8 percent.

It was recommended that Robert see James Schaller, MD, in
Tampa or Gael Wheeler, DO, in Tampa, for followup treatment of a possible Lymes or Babesia infection, in addition to the three apparent viral infections. Robert was treated by Dr. Schaller, for Lymes, Babesia and Bartonella.

Robert received 50,000 milligram intravenous Vitamin C, magnesium sulfate, glutathione, lidocaine and B vitamins, on 7/28/09. He did not appear to have dieoff symptoms, and was able to walk without a limp, with reduced air hunger, after the IV. He continued to have pain, in hands, knees and feet. He felt tired and went to sleep early.

On 7/29/09, Robert returned to Florida Detox for second Vitamin C IV, without cold packs. His ankles felt better and he rested quietly, during infusion. Taurine and Theanine were added to IV. Hands remained painful, appeared swollen,but feet and knees were less painful , and he appeared to be breathing easier.

Additional treatment has decreased pain and swelling in Robert’s hands and he is sleeping well.

On 8/24/09, after 13 intravenous Vitamin C treatments, Robert’s hands were not painful, if he avoided using them. His knee pain remained approximately 1/10. He could walk short distances, without pain and shortness of breath decreased, although he still used medical oxygen. His hands were cramping, if he used his fingers for more than very brief periods. Chills did not return, although sweats intensified. He was taking lumbrokinase four doses daily, to reduce clotting.

Lisa, Robert’s wife, reported her daughter has painful hands and feet, which occasionally turn blue, in cold water. It was explained that the daughter’s Reynauds symptoms might be due to a hereditary Factor V Leiden deficiency, which Robert was tested for.

I just have a few minutes but want to clarify a few things in which you mention my treatments. You were reported some errors. We all have this happen. It is why we have 13 tick infection books--our approaches can be read. Some of these can be read free and on Amazon.com. We have six Babesia books.

1) I have published in many of my tick infection books that ARTEMISININ is UTTER JUNK. I HAVE NEVER SUGGESTED IT--EVER.

And now even the top world malaria agencies have rejected for killing the easier to kill malaria. One thing for readers to note is that artesunate which I have promoted, e.g., in my pure Babesia clinical books and one ONLY on Sweet Wormwood or Artemisia, is listed under the category ARTEMISININ. Tricky and confusing to me so wanted to mention to others. Artemisinin is a semi-synthetic poor drug AND a category word in which artesunate is very good.

2) The dosages are people doing their own thing and not what is explained in SESSIONS. All tablets, liquids and capsules are started day 1-2 in small parts of the lowest dose made. We also do NOT run an assembly line or mill so and we have NO protocol. We tailor care like a wedding dress x 100. The report given you was anti-CUSTOM CARE.

3) We never start two things at once since even useful things like C and other IV things you mention can cause a reaction in unknown in potential patients. If IV magnesium 750mg can get a miserable reaction, anything can, and so the report to you of me starting all these AT ONCE sounds like folks we know who got some medicines, and went off on their own tear. Perhaps following 1995 approaches all over the blind net.

4) It is reported we raised a dose that was uncomfortable. This is sadistic, and we never would do something so markedly unkind. We do not tell people to JUST TOUGH OUT serious discomfort. And it sounds like they just did what they thought best, and did not use our 24/7 access where I could have fixed this trouble. It is Saturday 11 PM as I write this. We do not keep bankers hours.

I wish you great success as a top international addictionologist. And wish you success in the use of familiar functional medicine options to help people heal.

BTW. Nothing completely removes all mold inflammation chemicals or biotoxins. Period. CSM or cholestyramine clearly does not bind them all, as has been found in print in many places in the research from years ago. We also enhance liver function as one of many ways to move pathological chemicals out of the body.

AGAIN. THANKS GENIUS FOR OFFERING THE USA THE BEST AND CREATIVE ADDICTIONOLOGY MEDICINE AROUND. WE ARE PROUD OF YOU IN FLORIDA.

One of the obstacles is detection and identification of the disease syndromes. Lack of documentation of clinical suspicion and the difficulty in recognizing the causes is delaying the identification of these new diseases. The detection and follow up study of the infection's epidemiology will require huge investments and improvements in research.topical pain cream

My blood was sent to igenix lab in California since they are one of two labs in the US that specialize in detecting tick born illinesses. All other labs gave me negative results. I have babesiosis and lymes disease. I have most symptons but never had sweats or chills. I never had the bulls eye mark nor recall being bit by a tick. I'm trying to understand how I contracted these viruses though. I do remember swimming in a pool for about 20 minutes before I notices a dead rat at the bottom of the pool. Is there anyway I could have contracted these viruses from the pool??
Any feedback world be greatly appreciated!!

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